Shaanxi BLOOM Tech Co., Ltd. yog ib qho ntawm cov tuam ntxhab thiab cov muag khoom ntawm exenatide peptide hauv Suav teb. Txais tos rau cov lag luam wholesale bulk zoo exenatide peptide muag ntawm no los ntawm peb lub hoobkas. Kev pabcuam zoo thiab tus nqi tsim nyog muaj.
Exenatide Peptideyog ib qho khoom siv hluavtaws glucagon zoo li peptide-1 (GLP-1) receptor agonist, muaj cov saw peptide ntawm 39 amino acids. Nws cov qauv tshuaj muaj txiaj ntsig zoo ib yam li GLP-1 cov tshuaj hormone secreted los ntawm cov hnyuv, tab sis los ntawm kev ua kom zoo ntawm cov amino acid ib ntus, nws ua rau lub neej ntev ntev hauv vivo thiab txhim kho kev ruaj ntseg ntawm kev siv tshuaj. Nws yog nquag mus rau deamidation cov tshuaj tiv thaiv (Asn residue hloov mus rau Asp) nyob rau hauv kub los yog siab pH ib puag ncig, ua rau txo qis kev ua si. Nws thiab Trp residues yog oxidative degradation thiab yuav tsum tau nruj kev tiv thaiv los ntawm lub teeb thaum lub sij hawm cia. Cov peptide daim ntawv cog lus koom nrog hauv Asp yog qhov ua rau tawg nyob rau hauv alkaline tej yam kev mob, uas cuam tshuam rau cov tshuaj stability.
Peb Cov Khoom Muag Khoom







Exenatide / Exenatide acetate COA


Raws li lub ntiaj teb thawj pom zoo glucagon zoo li peptide-1 (GLP-1) receptor agonist,Exenatide PeptideFeem ntau yog siv rau kev kho mob ntshav qab zib hom 2. Nws lub luag haujlwm tsis txwv rau kev txo cov piam thaj kom meej thiab tswj qhov hnyav. Nyob rau hauv xyoo tas los no, kev tshawb fawb tau pom tias nws tuaj yeem tswj hwm lub siab biological moos los ntawm ntau txoj hauv kev los txhim kho daim siab metabolic atherosclerosis. Raws li lub hauv paus tseem ceeb ntawm lub cev metabolism, lub siab lub cev ua haujlwm (glucose thiab lipid metabolism, detoxification, lub zog hloov pauv, thiab lwm yam) raug tswj hwm los ntawm lub moos lom neeg. Cov kab mob ntawm lub siab biological moos yog ze ze rau hom 2 mob ntshav qab zib, uas tsis yog - haus dej cawv fatty siab kab mob (NAFLD), daim siab cirrhosis thiab lwm yam kab mob siab metabolic.
Cov khoom tseem ceeb thiab lub cev ua haujlwm ntawm lub siab circadian moos
Lub hauv paus tseem ceeb ntawm lub siab circadian moos yog cov lus txhais lus txhais lus tawm tswv yim voj (TTFL) tsim los ntawm cov noob caj noob ces, uas ua rau muaj kev cuam tshuam ntawm ntau txhiab cov noob hauv daim siab hlwb, yog li tswj hwm ntau yam kev ua haujlwm ntawm lub siab ntawm lub siab thiab ua tiav synchronous adaptation rau sab nraud ib puag ncig (lub teeb, zaub mov).
Cov lus pom zoo lub voj voog: Cov ntsiab lus tseem ceeb ntawm kev tswj hwm zoo yog CLOCK (clock ncig regulator) thiab BMAL1 (lub hlwb thiab cov leeg nqaij ARNT zoo li 1), ob qho tib si ntawm cov ntsiab lus tseem ceeb helix voj helix (bHLH) transcription yam. CLOCK tsim cov heterodimer nrog BMAL1, uas khi rau E- lub thawv khoom nyob rau hauv thaj tsam txhawb nqa ntawm cov noob caj noob ces, ua kom muaj kev tswj hwm tsis zoo thiab kev hloov pauv ntawm cov noob caj ces qis. Nws yog "core engine" uas tsav lub circadian atherosclerosis. Ntawm lawv, BMAL1 yog tus yuam sij rau kev tswj lub suab nrov, thiab nws cov kev hloov pauv raws sij hawm hauv cov theem qhia tau txiav txim siab qhov amplitude thiab lub sijhawm ntawm lub moos lom neeg.
Kev tawm tswv yim tsis zoo: Cov kev cai tseem ceeb tsis zoo suav nrog PER tsev neeg (Lub Sijhawm 1/2/3) thiab CRY tsev neeg (Cryptochrome 1/2). Tom qab lub CLOCK / BMAL1 complex qhib lub transcription ntawm PER thiab CRY noob, PER thiab CRY proteins yog synthesized thiab accumulated nyob rau hauv lub cytoplasm, thiab ces tsim heterodimers uas nkag mus rau hauv lub nucleus thiab khi rau lub CLOCK / BMAL1 complex, inhibiting nws transcriptional kev ua si thiab txo cov kev qhia ntawm nws tus kheej thiab downstream noob; Raws li PER thiab CRY cov proteins tau dhau los ua qhov kev puas tsuaj rau hauv ubiquitination, lawv cov teebmeem inhibitory maj mam tsis muaj zog, thiab CLOCK / BMAL1 complex reactivates transcription, ua tiav 24-teev cov lus tawm tswv yim voj.
Cov txheej txheem tswj hwm kev pabcuam: Ntxiv nrog rau cov noob caj noob ces, cov tswvcuab ntawm tsev neeg cov neeg txais kev pabcuam nuclear xws li REV-ERB / thiab ROR / / ua raws li cov cai tswjfwm pabcuam thiab koom nrog kev tswj hwm zoo ntawm TTFL. REV-ERB / tuaj yeem cuam tshuam BMAL1 kev qhia los ntawm kev khi rau RORE lub hauv paus hauv cheeb tsam BMAL1 txhawb nqa; ROR / / sib tw nrog REV-ERB los khi rau RORE cov ntsiab lus, ua kom BMAL1 qhia. Qhov sib npaug ntawm qhov sib npaug ntawm ob qho ntxiv stabilizes circadian atherosclerosis thiab txuas lub circadian atherosclerosis nrog cov txheej txheem metabolic.
Physiological functions ntawm daim siab circadian moos
Kev tswj cov piam thaj hauv cov metabolism: Lub siab lub cev moos tswj cov kev qhia ntawm cov piam thaj metabolism hauv cov noob los ntawm kev tswj hwm lub cev, ua tiav kev tswj hwm nruab hnub hmo ntuj ntawm cov ntshav qabzib homeostasis. Thaum nruab hnub (lub sijhawm pub mis), lub moos lom neeg ua rau kev qhia ntawm cov noob xws li glycogen synthase (GS) thiab glucokinase (GK) kom nce ntxiv, txhawb lub siab kev noj qab haus huv, synthesis ntawm glycogen, thiab txo cov ntshav qab zib; Thaum tsaus ntuj (lub sijhawm yoo mov), cov noob qhia ntawm glycogen phosphorylase (GP) thiab cov enzymes tseem ceeb gluconeogenesis (PEPCK, G6Pase) tau tswj hwm, txhawb nqa lub siab glycogen tawg thiab gluconeogenesis, tswj cov ntshav qabzib kom ruaj khov, thiab tsis txhob muaj cov piam thaj hauv cov ntshav.
Kev tswj hwm ntawm lipid metabolism: Lub siab lub cev moos tswj lub suab ntawm fatty acid synthesis, oxidation, thiab cov roj cholesterol metabolism. Thaum tsaus ntuj, qhov kev qhia ntawm fatty acid oxidation ntsig txog cov noob (PPAR, CPT1A) nce, txhawb cov fatty acid oxidation rau lub zog; Thaum nruab hnub, qhov kev qhia ntawm fatty acid synthesis ntsig txog noob (SREBP-1c, FAS) yog upregulated, txhawb fatty acid synthesis thiab cia. Nyob rau tib lub sijhawm, kev qhia ntawm cov roj cholesterol synthesis tseem ceeb enzyme (HMGCR) kuj qhia tau hais tias circadian atherosclerosis, synchronized nrog lub cev lipid yuav tsum tau.
Detoxification thiab bile acid metabolism: Lub siab ua haujlwm detoxification ntawm lub siab (xws li cov tshuaj metabolism thiab tshem tawm cov co toxins) yog tswj los ntawm lub moos lom neeg, thiab cov lus qhia ntawm cytochrome P450 tsev neeg (CYP450) cov tswv cuab (xws li CYP3A4, CYP2C9) muaj qhov tseem ceeb circadian atherosclerosis, nrog rau qhov muaj peev xwm tshaj tawm hmo ntuj thiab muaj zog tshaj plaws; Kev nthuav qhia ntawm cov enzyme tseem ceeb rau cov kua tsib acid synthesis (CYP7A1) kuj nthuav tawm lub circadian atherosclerosis, uas ua ke nrog kev noj zaub mov kom txhawb kev zom zaub mov thiab kev nqus.
Lub zog metabolism thiab kev tswj hwm autophagy: Lub siab lub sij hawm muaj feem cuam tshuam nrog mitochondrial zog metabolism, thiab kev qhia ntawm cov noob muaj feem xyuam rau mitochondrial oxidative phosphorylation muaj rhiab heev, kom ntseeg tau tias lub cev lub zog muab sib npaug rau qhov xav tau ntawm kev ua haujlwm nruab hnub thiab hmo ntuj; Nyob rau tib lub sijhawm, kev ua haujlwm ntawm daim siab autophagy kuj tseem tswj hwm los ntawm lub moos lom neeg, nrog rau kev nce ntxiv hauv autophagy thaum lub sijhawm yoo mov thaum hmo ntuj. Los ntawm degrading puas mitochondria (mitochondrial autophagy) thiab txawv txav proteins, daim siab cell homeostasis yog khaws cia, muab raw cov ntaub ntawv rau gluconeogenesis.
Cov ntaub ntawv pov thawj:
1. Molecular mechanism thiab metabolic kev tswj ntawm daim siab circadian moos Suav Journal of Hepatology, 2024
2. Circadian moos tswj nyob rau hauv daim siab: Mechanisms thiab metabolic cuam tshuam. Nature Reviews Gastroenterology & Hepatology, 2025.
3. Post transcriptional regulation mechanism ntawm insulin ntawm daim siab BMAL1 protein Suav Journal ntawm Biochemistry thiab Molecular Biology, 2024
4. Lub siab ua Nexus ntawm Txhua Hnub Metabolic Hla Sib Tham. Int Rev Cell Mol Biol, 2025.
5. Cov txheej txheem tswj hwm ntawm cov roj ntsha moos metabolism hauv autophagy axis cuam tshuam nrog cov kab mob Kev nce qib hauv Physiological Sciences, 2025
6. Insulin post-transcriptionally modulates Bmal1 protein cuam tshuam rau lub siab circadian moos. Pub Med, 2024
Lub ntsiab molecular mechanism ntawm Exenatide tswj lub siab circadian atherosclerosis
GLP-1 receptor yog ib tug tswv cuab ntawm G protein coupled receptor (GPCR) B tsev neeg, nthuav dav nyob rau saum npoo ntawm daim siab hlwb xws li parenchymal hlwb, hepatic stellate hlwb, thiab Kupffer hlwb. Nws cov lus qhia muaj qee yam circadian atherosclerosis thiab co tswj lub siab metabolism nrog lub siab circadian moos. Kev khi ntawmExenatide Peptiderau GLP-1 receptors nyob rau hauv daim siab yog lub hauv paus rau nws cov kev cai ntawm lub siab biological moos, thiab nws muaj cov yam ntxwv nram qab no:
High affinity thiab tshwj xeeb: Exenatide muaj qhov sib txawv tsis tu ncua (Kd) ntawm kwv yees li 0.3 nM nrog daim siab GLP-1 receptors, uas yog siab dua nyob rau hauv affinity tshaj natural GLP-1 (Kd ntawm kwv yees li 1.0 nM). Nws tsuas yog khi rau GLP-1 receptors thiab tsis hla khi nrog lwm cov receptors nuclear (xws li PPAR alpha thiab REV-ERB alpha), zam kev tawm tsam cov teebmeem thiab ua kom qhov tseeb ntawm kev tswj xyuas.
Rhythmic binding yam ntxwv: Kev khi ntawm Exenatide rau GLP-1 receptors muaj circadian atherosclerosis, synchronized nrog cov lus qhia atherosclerosis ntawm GLP-1 receptors hauv daim siab - thaum nruab hnub (lub sijhawm pub mis), theem qhia ntawm GLP-1 receptors hauv lub siab yog siab dua, thiab kev sib txuas nrog kev sib raug zoo ntawm Exenatide tseem ceeb dua, kev tswj hwm ntawm Exenatide tseem ceeb dua. Thaum tsaus ntuj (lub sijhawm yoo mov), receptor qhia qib txo qis, kev sib koom ua ke tsis muaj zog, thiab kev cuam tshuam ntau dhau ntawm lub siab circadian atherosclerosis thaum hmo ntuj (xws li cov piam thaj hauv siab thiab fatty acid oxidation) raug zam.

Kev txuas ntxiv ntawm receptor activation: Exenatide, nyob rau qib thib ob, yog glycine (Gly), uas tuaj yeem tiv thaiv cov enzymatic degradation ntawm dipeptidyl peptidase 4 (DPP-4), nrog ib nrab ntawm - lub neej txuas mus rau 2.4 teev. Tom qab txhaj tshuaj subcutaneous, nws tuaj yeem txuas ntxiv siv nws cov txiaj ntsig hauv lub cev, txuas ntxiv ua kom lub GLP-1 receptor nyob rau hauv daim siab, ua tiav cov kev cai mus sij hawm ntev ntawm lub siab biological moos, thiab tsis txhob muaj kev sib hloov ntawm lub cev.
Kev tshawb fawb tau pom tias khob tawm GLP-1 receptor nyob rau hauv lub siab tag nrho tshem tawm cov kev cai ntawm Exenatide ntawm lub siab circadian atherosclerosis, lees paub tias nws cov kev tswj xyuas nyob ntawm qhov ua kom GLP-1 receptors. Qhov no kuj yog ib qho ntawm cov yam ntxwv tseem ceeb uas teev Exenatide sib nrug los ntawm lwm cov tshuaj hypoglycemic xws li metformin thiab sulfonylureas.

Cov ntaub ntawv pov thawj:
1. Molecular mechanism kawm ntawm Exenatide tswj lub siab circadian atherosclerosis Suav Pharmacological Bulletin, 2024
2. Lub GLP-1 receptor agonist, Exenatide, Lub Sijhawm Tswjhwm Sib txawv cuam tshuam rau Circadian Rhythms hauv Diabetic db/db nas. University of Kentucky College of Medicine, 2024
3. Cov txheej txheem los ntawm exenatide inhibits pyroptosis thiab txhim kho cov kab mob siab insulin los ntawm PPAR delta BioTech, 2026
4. Exenatide ameliorates hepatic steatosis thiab attenuates fatty mass thiab FTO noob qhia los ntawm PI3K signaling pathway nyob rau hauv nonalcoholic fatty daim siab mob. PIB, 2024
5. Exenatide Attenuates Tsis yog-Alcoholic Steatohepatitis los ntawm Inhibiting Pyroptosis Signaling Pathway. Frontiers hauv Endocrinology, 2021
6. Cov txiaj ntsig kev tswj hwm thiab kev kho mob tseem ceeb ntawm GLP-1 receptor agonists ntawm daim siab circadian atherosclerosis Suav Journal of Endocrinology thiab Metabolism, 2024
Cov lus nug nquag
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A: Exenatide ua rau lub plab zom mov qeeb thiab inhibits plab hnyuv nqus. Nws tuaj yeem txo cov zis chylomicron postprandial nyob rau lub sijhawm luv luv, ua rau qhov tsis txaus ntseeg ntawm triglyceride nyeem uas tsis cuam tshuam qhov tseeb hauv qab lipid metabolism.
Q: Puas yog exenatide muaj kev cuam tshuam rau lub plawv dhia hloov pauv tsis muaj ntshav qabzib?
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A: Yog. Los ntawm kev ua kom lub hauv paus GLP-1 receptors, exenatide tuaj yeem ua kom cov suab nrov parasympathetic thiab txhim kho lub plawv dhia sib txawv. Cov nyhuv cardioprotective me me no yog ywj pheej ntawm kev txo cov piam thaj thiab poob phaus.
Q: Vim li cas exenatide tsis tshua muaj peev xwm ua rau muaj kab mob gallstone piv nrog semaglutide thiab liraglutide?
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A: Exenatide muaj cov nyhuv tsis muaj zog ntawm inhibiting gallbladder contraction. Nws luv luv ib nrab-lub neej thiab qis dua receptor activation siv ua rau cov kua tsib stasis tsawg, yog li qhov kev pheej hmoo ntawm cov pob zeb tsim muaj qis dua hauv cov ntaub ntawv kho mob.
Q: Exenatide puas tuaj yeem cuam tshuam rau pharmacokinetics ntawm levothyroxine?
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A: Yog. Nws ncua lub plab khoob thiab tuaj yeem txo qhov nqus ntawm qhov ncauj levothyroxine. Txawm hais tias nws tsis cuam tshuam rau cov theem tsis tu ncua, nws yuav ua rau qis qis T3 / T4 nyob rau thawj ob peb lub lis piam ntawm kev siv ua ke.
Q: Vim li cas exenatide qhia tsis muaj zog neuroprotective cuam tshuam hauv cov qauv tsiaj ntawm Parkinson tus kab mob?
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A: GLP-1 receptors tau nthuav dav hauv midbrain dopaminergic neurons. Exenatide tuaj yeem txo qhov ua kom microglial thiab oxidative kev nyuaj siab, tiv thaiv dopaminergic neurons. Cov nyhuv no tsis cuam tshuam nrog kev tswj ntshav qabzib.
Cim npe nrov: exenatide peptide, lwm tus neeg, manufacturers, hoobkas, lag luam wholesale, yuav, nqe, tej, kev muag khoom







